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Results for “neuronal plasticity”

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PubMed1999

The alpha7 nicotinic acetylcholine receptor in neuronal plasticity.

A growing body of evidence indicates that neuronal nicotinic acetylcholine receptors (nAChRs), in addition to promoting fast cholinergic transmission, may modulate other neuronal activities within the central nervous system (CNS). In particular, the alpha7 nAChR is highly permeable to Ca2+ and may serve a distinct role in regulating neuronal plasticity. By elevating intracellular Ca2+ levels in discrete neuronal locations, these ligand-gated ion channels may influence numerous physiological processes in developing and adult CNS. In this article, we review evidence that both pre- and postsynaptic alpha7 nAChRs modulate transmitter release in the brain and periphery through Ca2+-dependent mechanisms. The possible role of alpha7 nAChRs in regulating neuronal growth and differentiation in developing CNS is also evaluated. We consider an interaction between cholinergic and glutamatergic transmission and propose a hypothesis on the possible coregulation of intracellular Ca2+ by N-methyl-D-aspartate (NMDA) receptors and alpha7 nAChRs. Finally, the clinical significance of alterations in the normal function of alpha7 nAChRs is discussed as it pertains to prenatal nicotine exposure, schizophrenia, and epilepsy.

Animals↗

PubMed2000

Transcription-dependent neuronal plasticity: The nuclear calcium hypothesis.

In neurons, calcium ions control gene transcription induced by synaptic activity. The states and histories of neuronal activity are represented by a calcium code that comprises the site of calcium entry, and the amplitude, duration and spatial properties of signal-evoked calcium transients. The calcium code is used to transform specific firing patterns into qualitatively and quantitatively distinct transcriptional responses. The following hypothesis is proposed: electrical activity causes long-lasting, transcription-dependent changes in neuronal functions when synaptically evoked calcium transients associated with the stimulation propagate to the nucleus; gene transcription activated by dendritic calcium signals only is insufficient to consolidate functional alterations long-term. Similar to enduring increases in synaptic efficacy, nuclear calcium transients are induced by high-frequency firing patterns or by weak synaptic inputs coinciding with backpropagating dendritic action potentials. Nuclear calcium stimulates CREB-mediated transcription and, through inducing the activity of the transcriptional coactivator CREB-binding protein (CBP), may modulate the expression of numerous genes including neurotransmitter receptors and scaffolding proteins. Increases in the transcription rate of target genes are predicted to be transient and in many cases small, however, they collectively contribute to the maintenance of changes in synaptic efficacy. Nuclear calcium may be the common regulator of diverse transcription-dependent forms of neuronal plasticity.

Animals↗

PubMed2006

[Progress and investigation of neuronal plasticity interfered by Borna disease virus infection].

Borna disease virus (BDV) is highly neuronotropic. Recently, more and more investigations indicated that BDV infection was close related to human neuropsychic disorders. However, the mechanism underlying the disorders was unclear to date. Some investigators thought neuronal plasticity changes by BDV infection in the central nervous system may be it's cardinal basis. Many researchers have studied the molecular mechanisms, which might lead to disturbances in neuronal plasticity by BDV infection, through infection-based animal modes such as gerbils modes, rats modes, mice modes and transgenic mice modes. The results showed that neuronal plasticity was interfered by BDV infection through interference with trophic support from astrocytes to neurons, interference with amphoterin signaling and interference with neurotrophin signaling. The disturbances in neuronal plasticity would result in cerebral disorders and cause behavior alterations and psychic alterations of host. In the following years, the ability to manipulate the BDV genome may help uncover unrecognized aspects of the basic mechanisms operating in the regulation of neuronal plasticity of interference with neuronal physiology caused by BDV, give academic foundation for clinical prevention and therapy of BD.

Animals↗

PubMed1998

Neuronal activity induction of the stathmin-like gene RB3 in the rat hippocampus: possible role in neuronal plasticity.

Synaptic activity induces a rapid transcriptional response that is essential for the establishment of long-term neuronal plasticity. Using a differential cloning technique, we have identified a gene induced by seizure activity in the brain as RB3. RB3 is a recently cloned gene belonging to the stathmin family of phosphoproteins. Like SCG10, RB3 is brain-specific, although in situ hybridization results show that the expression of RB3 is more ubiquitous than is that of SCG10. Using genomic DNA sequencing, we show that the 27 amino acid sequence unique to the RB3" transcript is encoded by an alternatively spliced exon, exon 2'. Using a peptide antibody raised against exon 2' to detect RB3" and an anti-Flag antibody to detect an epitope-tagged version of RB3, we show that both proteins are localized to the Golgi apparatus of transfected COS7 cells. Of particular interest, RB3 mRNA, but not SCG10 mRNA, is rapidly induced in the dentate gyrus granule layer of the hippocampus after electrically induced seizure activity as well as stimuli leading to long-term potentiation (LTP). In addition, RB3 mRNA is induced in pheochromocytoma (PC12) cells treated with 250 ng/ml NGF. These results suggest that RB3 may play a role in activity-induced neuronal plasticity and neuronal differentiation.

Alternative Splicing↗

PubMed2001

Developmental disorders of activity dependent neuronal plasticity.

A number of neurodevelopmental disorders are caused by defects in activity dependent neuronal plasticity, the process by which neuronal activity shapes developing neuronal circuits. These disorders are caused by genetic mutations or other factors that disrupt intracellular signaling pathways that link the cell surface with the nuclear machinery for gene expression. The signaling pathways disrupted by these disorders are involved in learning, memory and behavior as well as in the synaptic proliferation and pruning that occurs during normal development. Examples of neurodevelopmental disorders that target plasticity include X-linked disorders such as Rett, Fragile-X and Coffin-Lowry Syndromes as well as acquired disorders such as cretinism. Several other X-linked mental retardation syndromes as well as autosomal disorders including neurofibromatosis type 1 and tuberous sclerosis also involve signaling pathways involved in neuronal plasticity. Disruption of neuronal plasticity is a mechanism that may underlie a diverse group of neurodevelopmental disorders.

Brain Diseases↗

PubMed2006

Mitochondrial regulation of neuronal plasticity.

The structure and function of neurons is dynamic during development and in adaptive responses of the adult nervous system to environmental demands. The mechanisms that regulate neuronal plasticity are poorly understood, but are believed to involve neurotransmitter and neurotrophic factor signaling pathways. In the present article, I review emerging evidence that mitochondria play important roles in regulating developmental and adult neuroplasticity. In neurons, mitochondria are located in axons, dendrites, growth cones and pre- and post-synaptic terminals where their movements and functions are regulated by local signals such as neurotrophic factors and calcium influx. Mitochondria play important roles in fundamental developmental processes including the establishment of axonal polarity and the regulation of neurite outgrowth, and are also involved in synaptic plasticity in the mature nervous system. Abnormalities in mitochondria are associated with neurodegenerative and psychiatric disorders, suggesting a therapeutic potential for approaches that target mitochondrial mechanisms.

Aging↗

PubMed1996

[Neuronal plasticity].

The term 'brain plasticity' means the brain capacity to diminish the effects of the lesions through structural functional changes. A great part of the pathological processes of the nervous system affecting the corticospinal and the subcorticospinal tracts, the cerebellar, spinal, visual, language and other systems show neuronal plasticity, spontaneously in some cases and after suitable rehabilitation in others. The clinical manifestations of neuronal plasticity are observed especially after prenatal, neonatal or childhood cerebral damage. During the adulthood, the brain has less capacity of neuronal plasticity, although plastic changes may be found at any age. Apart the clinic, the neuronal plasticity can be studied through electrophysiology, MR, positron emission tomography (PET), transcranial magnetic stimulation (TME), and obviously by histology, this latter especially in experimental studies. In pediatric Neurology, the concept of brain plasticity is frequently used to explain the favourable clinic evolution in a lot of cases with severe brain injury.

Age Factors↗

PubMed1993

Calcium and neuronal plasticity.

The proposed involvement of free intracellular calcium concentration ([Ca]i) in neuronal plasticity is examined. While it is generally believed that a rise of [Ca]i is necessary for the triggering of long-term modification of synaptic connections, there are many unresolved issues related to this dogma; it is not entirely clear what is the source of the elevated calcium, how much of a calcium rise is sufficient to produce the synaptic potentiation, where and for how long, and what are the relevant chemical consequences of the transient rise of [Ca]i. It is generally believed that the dendritic spine is the locus of synaptic modification, yet little evidence exists to support this view. High resolution calcium imaging studies may contribute to the clarification of some key issues in the field of neuronal plasticity.

Animals↗

PubMed2001

The role of neurotrophic factors in psychostimulant-induced behavioral and neuronal plasticity.

Several neurotrophic factors influence the development, maintenance and survival of dopaminergic neurons in the mammalian central nervous system (CNS), including neurotrophin-3 (NT-3), brain derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF), basic fibroblast growth factor (bFGF) and glial derived neurotrophic factor (GDNF). This review focuses on the role of these neurotrophic factors in psychostimulant-induced behavioral sensitization, a form of dopamine-mediated neuronal plasticity that models aspects of paranoid schizophrenia as well as drug craving among psychostimulant addicts. Whereas NT-3, CNTF and bFGF appear to play a positive role in psychostimulant-induced behavioral sensitization, GDNF inhibits this form of behavioral plasticity. The role of BDNF in behavioral sensitization, however, remains elusive. While it has been shown that neurotrophic factors can influence the behavioral, structural and biochemical phenomena related to psychostimulant-induced neuronal plasticity, it is unclear which neurotrophic factors are important physiologically and which have purely pharmacological effects. In either case, examining the role of neurotrophic factors in behavioral sensitization may enhance our understanding of the mechanisms underlying the development of paranoid psychosis and drug craving and lead to the development of novel pharmacological treatments for these disorders.

Animals↗

PubMed1995

Mechanisms of neuronal plasticity as analyzed at the single cell level.

This chapter has highlighted how correlates of neuronal plasticity such as electrophysiological responsiveness and changes in gene expression may be examined in defined CNS regions as well as in single cells. The ability to simultaneously measure the mRNA levels for hundreds of different genes, to clone novel genes, and to characterize the physiology and morphology of the cell promises to provide insight into molecular mechanisms of plasticity. The importance of understanding how one gene product changes relative to another (coordinated changes) as well as subcellular distribution of mRNAs cannot be overstated. It is only through an analysis of both the molecular and cellular processes associated with plasticity that a thorough understanding of the mechanisms of neuronal plasticity can be gained.

Animals↗

PubMed2001

Aluminum promotes neuronal plasticity events in a mouse neuroblastoma cell line.

The effects of aluminum(III) on microtubular meshwork have been investigated using cultured murine neuroblastoma cells grown in a medium containing aluminum lactate at defined metal concentrations (10-20 microM). A role of aluminum(III) in promoting neuronal plasticity events is suggested. These events including sprouting and neurite outgrowth are associated with an increased tyrosine-tubulin (Tyr-Tub) expression, which can be due to the enhanced needs of recently formed, highly dynamic microtubules typical of neuronal plasticity. After 48 and 72 h aluminum exposure, an upregulation of Tyr-Tub expression is detected and this is concentration-dependent. A high amount of Tyr-Tub is observed also in non-treated cells, although later than in aluminum-exposed cells. Thus, it is possible that aluminum(III) accelerates neuronal plasticity events, for which Tyr-Tub is confirmed to be a useful marker.

Aluminum↗

PubMed2005

Standard three-dimensional glomeruli of the Manduca sexta antennal lobe: a tool to study both developmental and adult neuronal plasticity.

The metamorphosing antennal lobe (AL) of the sphinx moth Manduca sexta serves as an established model system for studying neuronal development. To improve our understanding of mechanisms involved in neuronal plasticity, we have analyzed the size, shape, and localization of ten identified glomeruli at three different time points during development and in the adult, viz., (1) 13 days after pupal eclosion (P13), which reflects a time when the basic glomerular map has formed, (2) immediately after adult eclosion (A0), which represents a time when the newly formed glomeruli are uninfluenced by external odors, and (3) 4 days after adult eclosion (A4), which reflects a time when the animals have been exposed to surrounding odors. Our data from normally developing ALs of male M. sexta from P13 to A0 revealed an increase in size of all examined glomeruli of between 40% and 130%, with the strongest increases occurring in two of the three sex-specific glomeruli (cumulus, toroid). From A0 to A4, the cumulus and toroid increased significantly when correlated to AL volume, whereas the other glomeruli reached the sizes gained after A0. This study was based on antibody staining against the ubiquitous synaptic vesicle protein synaptotagmin, confocal laser scan microscopy, and the three-dimensional (3D) analysis tool AMIRA. Tissue permeability and therefore reliability of the staining quality was enhanced by using formalin/methanol fixation. The standard 3D glomeruli introduced in this study can now be used as basic tools for further examination of neuronal plasticity at the level of the identified neuropil structures, viz., the glomeruli of the AL of M. sexta.

Animals↗

PubMed2005

Neuronal plasticity, stress and depression: involvement of the cytoskeletal microtubular system?

In susceptible individuals, stressors can increase the risk of onset of depression and recent brain imaging studies have shown morphometric alterations in the limbic system of patients affected by depression. The volume loss observed in the hippocampus of depressed individuals suggests a possible involvement of structural neuronal plasticity in the pathogenesis of depression. Stressful conditions in animals can result in impaired structural neuronal plasticity in the hippocampus, characterised by retraction of apical dendrites and decreased neurogenesis. The intrinsic dynamic instability of the cytoskeletal microtubular system is essential for neuronal remodelling and plasticity. We have recently shown that both acute and chronic stress decrease microtubular dynamics in the rat hippocampus. Other authors have demonstrated that proteins functionally involved in the regulation of microtubule dynamics can be altered by stress in the rodent hippocampus. Furthermore, the existence of a link between stress-induced microtubular changes and depression is further strengthened by evidence showing that both acute and chronic treatment with antidepressant drugs can affect the expression of microtubular proteins. The present review will introduce a growing body of evidence suggesting that stress-induced alterations in neuronal plasticity might be considered the final result of activation and/or inhibition of molecular cascades regulating the dynamics of the microtubular system. In addition, the prospect of targeting microtubules as a pharmacotherapeutic approach to treat mood disorders will be discussed.

Animals↗

PubMed2002

Aging and neuronal plasticity: lessons from a model.

In spite of many well-documented examples of age-related reductions in neuronal plasticity, the causes of such changes remain largely unknown. One example of age-reduced plasticity involves an aberrant sprouting response of mature rat sympathetic neurons into the CNS (hippocampal formation). This phenomenon has proven to be useful for exploring the relative contribution of target aging (extrinsic influences) versus neuronal aging (intrinsic influences) to reduced sprouting. Aged sympathetic neurons mount a robust growth response when confronted with young target tissue or when exposed to exogenous trophic factor in vivo. In contrast, the aged target tissue (the hippocampal formation in this example) exhibits reduced receptivity for sympathetic sprouting. This change in the target does not appear to be due to alterations in baseline levels of trophic or substrate support for axonal growth. Rather, aging appears to dampen the consequences of target denervation so that the aged target elicits less sprouting. Age-related reductions in neuronal sprouting are speculated to reflect increasing commitment to information storage at the expense of neuronal plasticity.

Aging↗

PubMed2006

Neuronal differentiation is accompanied by increased levels of SNAP-25 protein in fetal rat primary cortical neurons: implications in neuronal plasticity and Alzheimer's disease.

Alzheimer's disease (AD) is accompanied by progressive memory loss and decline in general cognitive abilities. Neuropathological hallmarks include amyloid plaque formation, neurofibrillary tangles, and neuronal and synaptic loss. To improve research models in AD, we have characterized several aspects of the primary rat neuronal cell culture model, which relate directly to the study of neuroexocytosis, neuronal plasticity, and amyloidosis. We have attempted to isolate and assess the neuronal enrichment of a primary cortical cell culture by morphological and molecular techniques, following progress of these cultured cells for up to 18 days in culture to identify the optimum timeframe for the manipulation and data collection in these cells. We observed maximum neuronal differentiation around day 15, which was in decline by day 18, thus, the critical window for manipulations in these cultures seems to be between days 12-15. The substantial increase in neuritic length and density was apparent at very early time points and peaked at day 15. In parallel to morphological assessments, we measured levels of a group of selected neuronally important proteins, including cytoskeletal and synaptic proteins. Change in the levels of cell-associated APP and synaptophysin were not as dramatic as that of SNAP-25 or secreted APP. Notably, this increased differentiation is accompanied by a dramatic increase in levels of SNAP-25 protein, which peaked at day 15 and declined thereafter. These results suggest that this neuronal population contains quantifiable presynaptic terminals. Thus, the establishment and molecular characterization of this neuronal model would have many implications in neuroscience research including synaptic differentiation and neuronal plasticity and for the evaluation of pharmacological interventions in the disease process.

Alzheimer Disease↗

PubMed2005

Borna disease virus interference with neuronal plasticity.

Viruses able to infect the central nervous system (CNS) are increasingly being recognized as important factors that can cause mental diseases by interfering with neuronal plasticity. The mechanisms whereby such infections disturb brain functions are beginning to emerge. Borna disease virus (BDV), which causes a persistent infection of neurons without direct cytolysis in several mammalian hosts, has recently gained interest as a unique model to study the mechanisms of viral interference with neuronal plasticity. This review will summarize several hypotheses that have been put forward to explain possible levels of BDV interference with brain function.

Animals↗

PubMedDate not supplied

[The effect of changes in the dynamic equilibrium in the microtubular and microfilamentous systems on neuronal plastic reactions].

Effects of disruption or stabilization of microfilaments or microtubules on formation of neuronal plastic reactions (NPR) were studied in isolated Lymnaea stagnalis neurons. Disruption of these cytoskeletal elements blocked the development of the NPR. After stabilization of the microtubules the dynamics of development and retention of the NPR became dependent on the stimulation series. Stabilization of the microfilaments blocked the development but improved the retention of the NPR. The role of the dynamic cytoskeletal reorganization in the process of NPR formation is discussed on the basis of the obtained data.

Actin Cytoskeleton↗

PubMed1995

Neurotrophins and neuronal plasticity.

There is increasing evidence that neurotrophins (NTs) are involved in processes of neuronal plasticity besides their well-established actions in regulating the survival, differentiation, and maintenance of functions of specific populations of neurons. Nerve growth factor, brain-derived neurotrophic factor, NT-4/5, and corresponding antibodies dramatically modify the development of the visual cortex. Although the neuronal elements involved have not yet been identified, complementary studies of other systems have demonstrated that NT synthesis is rapidly regulated by neuronal activity and that NTs are released in an activity-dependent manner from neuronal dendrites. These data, together with the observation that NTs enhance transmitter release from neurons that express the corresponding signal-transducing Trk receptors, suggest a role for NTs as selective retrograde messengers that regulate synaptic efficacy.

Animals↗